The Effects of Intentional Changes of Brain Temperature on The Experimental Brain Contusion

本课题研究了有意改变脑温对实验性脑挫伤的影响。1995年，我们首先对72 kDa热休克蛋白（HSP 72）作为神经元损伤标志物的免疫组化表达进行了初步研究。对成年雄性大鼠进行侧向流体肿胀性损伤。损伤大鼠分为常温组（37.0-37.5 ℃）和低温组（30.0-31.5 ℃）。分别于伤后24、48、72小时行免疫组化检测。结果表明，两组大鼠海马HSP 72阳性神经元均以24小时最明显，但低温组明显少于常温组。本研究初步提示亚低温对脑损伤具有保护作用。根据这些结果，我们于1996年制定了一个计划，以评估故意改变脑温度对血脑屏障（BBB）破坏和胶质反应的影响。但在1995年初步研究完成后，出现了一些问题，影响了下一步的计划：（1）液体冲击损伤装置和振动刀的故障。2)非预期的非特异性背景染色。3)新的冷热法和硬膜外温度传感器置入后颅窝等技术问题。4)旧（1995）和新（1996）损伤模型之间脑损伤形成差异的可能性。结果：在22只治疗组大鼠中，只有3只大鼠（34 ℃组= 2，37 ℃组=1）在伤后24小时可以评价HSP 72的表达和胶质反应。结果表明，亚低温（34 ℃）对HSP 72的表达和小胶质细胞的活化无明显影响，而对星形胶质细胞的反应性则明显降低。

In this project, we investigated the effects of intentional changes of brain temperature on the experimental brain contusion. Firstly as a preliminary study, in 1995, we evaluated the immunohistochemical expression of 72 kDa heat shock protein (HSP72) as a marker of neuronal damage. Adult male rats were subjected to a lateral fluid percussive injury. Injured rats were divided into two groups ; normothermic group (37.0-37.5ﾟC) and hypothermic group (30.0-31.5ﾟC). The immunohistochemical evaluation was performed at 24,48, and 72 hours after injury. The results showd that HSP72-positive neurons were observed most prominently at 24 hours in both groups but their numbers in hypothermic group were significantly less than those in normothermic group. This preliminary study suggested that the protective effects of moderate hypothermia on the injured brain. According to these results, in 1996, we made a plan to evaluate the effects of intentional changes of brain temperature on blood-brain barrier (BBB) disruption and glial response. However, after the completion of the preliminary study in 1995, some problems which disturbed the next plan occured : 1) The breakdown of fluid percussive injury device and vibratome. 2) Unexpected non-specific background staining in immunohistochemisty. 3) Technical problems such as new cooling-heating method and insertion of epidural thermosenser into posterior fossa. 4) The possibility of difference in brain injury formation between old (1995) and new (1996) injury model. As a result, among 22 treated rats, we could evaluate only three rats (34ﾟC group=2,37ﾟC group=1) concerning to expression of HSP72 and glial response at 24 hours after injury. The results showed that there were no obvious effects of mild hypothermia (34ﾟC) on expression of HSP72 and microglial activation, whereas astrocytic responses were seemd to decrease in mild hypothermic group.